Improved immunosuppression should avoid early steroid bolus therapy after transplantation. A low platelet count promotes herniation. Transverse abdominal incision seems to be the best approach for liver transplantation. Prosthetic hernia repair does not increase the complication rate.

End-stage liver disease is being treated by liver transplantation. Despite legislative and social efforts, the number of cadaveric organs suitable for liver transplantation has not grown to match the increasing demand. The insufficient number of grafts results in high mortality for patients on the waiting list and prolonged waiting times with increasing morbidity. Following the success of living related-donor segmental liver transplantation in children, an amended concept has been applied to the adult patients. The early experience with this technique, the process concerning the selection of the donor for the recipient, the risks of the donor, and the future evolution of living related-donor liver transplantation are the topics of this article.

Splanchnic vasodilatation and vascular hyporesponsiveness to vasopressors are characteristic features of patients with cirrhosis. Although the vascular response to different vasopressors has been shown to be attenuated in cirrhosis, alterations on the receptor level are discussed controversially. Thus, impaired postreceptor signaling has been postulated. However, so far this has not been studied in human splanchnic vessels. Therefore, we assessed the vascular response of human hepatic arteries after activating the G-protein-dependent signal transduction pathway by stimulation with angiotensin II, the thromboxane A 2 analog U46619, or by G-protein activation with NaF/AlCl 3 . After endothelium denudation, cumulative isometric concentration contraction curves were obtained for hepatic arteries from 32 cirrhotic patients undergoing liver transplantation and from 40 organ donors after stimulation with either angiotensin II (10 ؊11 -10 ؊5 mol/L), U46619 (10 ؊10 -10 ؊6 mol/L) or AlCl 3 (30 mol/L)/NaF (10 ؊4 -3 ؋ 10 ؊2 mol/L). Hepatic arteries from cirrhotic patients were markedly less responsive to angiotensin II (P < .0001) than those from organ donors. Both stimulation of the G-protein phospholipase C pathway via the thromboxane A 2 receptor and receptor-independent Gprotein stimulation with AlCl 3 /NaF, induced an intact contractile response. In conclusion, the G-protein-dependent signal transduction system itself is unaltered in cirrhosis. Hence, the cause of the hyporesponsiveness to some vasoconstrictors in cirrhosis appears to be a receptor-specific phenomenon localized upstream from the G-protein level. (HEPATOLOGY 2001;34:884-888.)Peripheral and splanchnic vasodilatation leading to hyperdynamic circulation are characteristic hemodynamic features in patients with cirrhosis and in animal models with portal hypertension. 1-3 Supposedly, this is caused by an impaired vascular response to different vasoconstrictors as found in animal models with cirrhosis. [4][5][6][7][8][9][10] Recently, hyporesponsiveness of human hepatic arteries from patients with cirrhosis to vasoconstrictors such as the ␣ 1 -agonist methoxamine, 11 vasopressin, 12 or 5-hydroxytryptamine 12 has also been found. However, the exact pathophysiologic basis of the vascular hyporesponsiveness in cirrhosis has so far not been elucidated. Because vascular hyporesponsiveness has been shown to persist after inhibition of nitric oxide synthesis and endothelium removal 11,13 it cannot be solely explained by increased formation of nitric oxide in cirrhosis.Vascular hyporeactivity in cirrhosis involves different Gprotein-linked transmembrane receptors including the ␣ 1 -adrenoceptor, 6,10,11 the angiotensin II type 1 (AT 1 ) receptor, 5,14-16 and the vasopressin receptor. 12 Stimulation of these receptors predominantly induces smooth muscle contraction by G-protein (␣-subunit)-dependent activation of phospholipase C (PLC). This catalyzes formation of inositol 1,4,5-triphosphate (IP 3 ) and 1,2-diacylglycerol, which induces Ca 2ϩ mobilization and protein ki...

SUMMARY BackgroundCalcineurin inhibitor (CNI)-related nephrotoxicity significantly contributes to chronic renal failure after liver transplantation.

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A 1-yr-old child presented with intractable right sided pleural effusion and progressive clinical deterioration 3 weeks after liver transplantation for Alagille Syndrome. He had been treated successfully for severe acute rejection before. Ultrasound and Doppler mode studies repeatedly demonstrated air in the portal vein. Intra-abdominal and intra-thoracic lymphoproliferation was detected, and EBV virus load and serology were suggestive of primary EBV infection. Liver biopsy revealed blast-like infiltrates of B-cells, considered diagnostic for post-transplant lymphoproliferative disease. The disease resolved upon reduction of immunosuppression. We suggest that the detection of portal vein gas in pediatric liver transplant recipients beyond the early post-operative period may be a sign of intra-abdominal post-transplant lymphoproliferative disease.